ライフサイエンスコーパス: bladder carcinoma

1 cancer progression in patients with stage T1 bladder carcinoma.

2 risk population of patients with superficial bladder carcinoma.

3 11 with bile duct cancer and four with gall-bladder carcinoma.

4 t efficient adjuvant therapy for superficial bladder carcinoma.

5 ble tools for cytopathological screening for bladder carcinoma.

6 es than to UTUC, which is similar to that of bladder carcinoma.

7 cterial infection and early-onset metastatic bladder carcinoma.

8 versely correlated with LSD1 levels in human bladder carcinoma.

9 ed as an effective treatment for superficial bladder carcinoma.

10 in moderately VSV-resistant liposarcoma and bladder carcinoma.

11 The most common secondary malignancy is bladder carcinoma.

12 eeded to detect occult metastatic disease in bladder carcinoma.

13 is admixed with other histological types of bladder carcinoma.

14 ed with a monoclonal antibody raised against bladder carcinoma.

15 s potential as a therapeutic target in human bladder carcinoma.

16 samples of nearly all patients with urinary bladder carcinoma.

17 in 10 primary colon carcinomas and eighteen bladder carcinomas.

18 und in late-stage and high-grade ovarian and bladder carcinomas.

19 splasias, multiple myeloma, and cervical and bladder carcinomas.

20 t in poorly differentiated glioblastomas and bladder carcinomas.

21 d bone and in the majority of human lung and bladder carcinomas.

22 n, MiaPaCa pancreatic, Calu-1 lung, and EJ-1 bladder carcinomas.

23 NTRK and FGFR gene families were detected in bladder carcinoma (3.3%), glioblastoma (4.4%), head and

24 e activity) as well as antitumoral agents in bladder carcinoma 5637.

25 ve dramatically suppressed subcutaneous MB49-bladder carcinoma and B16-melanoma growth and prolonged

26 in plasma was also observed in non-invasive bladder carcinoma and I-BLCA.

27 e conclude that FGFR3 is commonly mutated in bladder carcinoma and only rarely in cervical carcinoma.

28 ab exerted potent antitumor activity against bladder carcinoma and t(4;14)-positive multiple myeloma

29 nd smoking are at particular risk to develop bladder carcinomas and support the need for long-term ca

30 nvasive phenotype in melanomas and colon and bladder carcinomas and with the metastatic phenotype in

31 nd neck squamous cell carcinoma cells); T24 (bladder carcinoma); and DU 145 (prostate carcinoma).

32 n human cancers, including multiple myeloma, bladder carcinoma, and cervical cancer.

33 357 pancreatic carcinoma cells in G2/M, T-24 bladder carcinoma, and HT-1080 fibrosarcoma cells in G0/

34 significant number of patients with stage T1 bladder carcinoma are at risk for cancer progression.

35 vels of KiSS-1 were observed in the invasive bladder carcinomas as compared to superficial tumors.

36 biology and treatment, clinical outcomes of bladder carcinoma (BC) patients are still not satisfacto

37 rat cell lines of nonhematopoietic lineage (bladder carcinoma BC47 and gliosarcoma 9L).

38 porine did not induce G1 phase arrest in the bladder carcinoma cell line 5637 that lacks a functional

39 Induction of wild-type p53 in the ECV-304 bladder carcinoma cell line by infection with a p53 reco

40 lines with mutations in either H-ras (human bladder carcinoma cell line T24 and mouse keratinocyte c

41 3 and Ha-ras mutations identical to those in bladder carcinoma cell line T24 prompted us to investiga

42 prostatic origin but are derivatives of the bladder carcinoma cell line T24.

43 mplicated in N-cadherin-mediated invasion in bladder carcinoma cell lines revealed no correlation bet

44 Examination of bladder carcinoma cell lines reveals that certain lines

45 n this group, we used a preclinical model of bladder carcinoma cell lines to study a unique SV (trans

46 id human lung fibroblasts (MRC-5), and human bladder carcinoma cell lines with (T24) or without (J-82

47 Secreted miRNA characterized from isogenic bladder carcinoma cell lines with differing metastatic p

48 at FGFR3 functions as an important driver of bladder carcinoma cell proliferation (see the related ar

49 ibitor of both normal bladder epithelial and bladder carcinoma cell proliferation.

50 hine decarboxylase (ODC) activity with human bladder carcinoma cells (T24 cells), and TPA-induced nuc

51 on in cytoplasmic extracts prepared from T24 bladder carcinoma cells and human embryo fibroblasts sta

52 Two APF-responsive cell lines (T24 bladder carcinoma cells and the immortalized human bladd

53 t that inducible knockdown of FGFR3 in human bladder carcinoma cells arrested cell-cycle progression

54 t of human non-small cell lung carcinoma and bladder carcinoma cells by a recombinant adenovirus vect

55 es Akt as a modulator molecule in protecting bladder carcinoma cells from TRAIL-induced apoptosis.

56 shown to exhibit antitumor activity in human bladder carcinoma cells in vitro and in mouse bladder ca

57 eration of normal bladder epithelial and T24 bladder carcinoma cells in vitro by binding to cytoskele

58 ristate 13-acetate (PMA)] treatment of human bladder carcinoma cells induced S198 phosphorylation of

59 ly induce replicative senescence in EJ human bladder carcinoma cells lacking functional p53.

60 Human bladder carcinoma cells mutant for p53 and containing a

61 Overexpression of galectin-3 in J82 human bladder carcinoma cells rendered them resistant to TRAIL

62 Through transcriptional profiling of bladder carcinoma cells subjected to short hairpin RNA k

63 growth factor (CTGF/CCN2) expression in T24 bladder carcinoma cells treated with APF.

64 ression of PKC-alpha protein and mRNA in T24 bladder carcinoma cells was reduced by approximately 80

65 mportant in lung metastasis, lung metastatic bladder carcinoma cells were injected in mice treated wi

66 We treated T24 bladder carcinoma cells with 5-Aza-2'-deoxycytidine to i

67 +1 bp resulted in preferential expression in bladder carcinoma cells with negligible expression in no

68 ressed the B-myb promoter in EJ cells (human bladder carcinoma cells), which have a functional Rb, bu

69 in response to HSP90 inhibitor treatment in bladder carcinoma cells, and thus intensifies the unders

70 noculated s.c. with 5 x 10(4) syngeneic MB49 bladder carcinoma cells, and tumor growth was quantitate

71 In T24 bladder carcinoma cells, SAHA induces up to a 9-fold inc

72 In T24 human bladder carcinoma cells, these EGSs, but not control seq

73 es, in both LD419 normal fibroblasts and T24 bladder carcinoma cells, whereas the acetylation changes

74 tem, that wild-type p53 overexpression in EJ bladder carcinoma cells, which have lost functional p53,

75 ipheral blood mononuclear cells (PBMCs), and bladder carcinoma cells.

76 whereas high doses induced apoptosis in T24 bladder carcinoma cells.

77 profiling the expression of RalA/B-depleted bladder carcinoma cells.

78 tably transfected into E-cadherin expressing bladder carcinoma cells.

79 butes to the increased invasive potential of bladder carcinoma cells.

80 identified in several tumour types including bladder carcinoma, cervical carcinoma, and multiple myel

81 cient to drive both noninvasive and invasive bladder carcinoma development in transgenic mice.

82 butyl-N-(4-hydroxybutyl) nitrosamine-induced bladder carcinoma development.

83 frequent abnormalities have been observed in bladder carcinoma, esophageal cancers, and several other

84 visualization of malignant lesions in human bladder carcinoma ex vivo.

85 lung carcinoma (seven patients, 15.6%), and bladder carcinoma (four patients, 8.9%).

86 mCD40L versus soluble CD40L (sCD40L) on T24 bladder carcinoma gene expression profiling.

87 ) = 0.71 [0.60-0.85], p = 0.0002, urothelial bladder carcinoma: HR = 0.74 [0.59-0.93], p = 0.01, and

88 tumor blood vasculature from human invasive bladder carcinoma (I-BLCA) and normal bladder tissue vas

89 eic mice and in blocking the growth of human bladder carcinoma implanted in nude mice.

90 e post-translational modifications (PTMs) in bladder carcinoma in response to HSP90 inhibition.

91 we have profiled the expression of miRNAs in bladder carcinoma in situ (CIS) and distinct cell compar

92 low copy number of SV40T transgene developed bladder carcinoma in situ (CIS), whereas those bearing h

93 Uterine and bladder carcinoma induced by arsenic plus diethylstilbes

94 ~25,000 cells) of RT112 cells (derived from bladder carcinoma), induces a near-uniform intracellular

95 travesicular administration in patients with bladder carcinoma, initially using [123I]IUdR and curren

96 We show that growth of B16 melanoma and MB49 bladder carcinoma is reduced in IL-17(-/-) mice but dras

97 e, in two human cancer cell lines; UMUC-3, a bladder carcinoma line, and the prostate carcinoma line,

98 A) suppresses the proliferation of the human bladder carcinoma line, T24.

99 Muscle-invasive bladder carcinomas (MIBCs) are aggressive genitourinary

100 ity is a promising tool for the diagnosis of bladder carcinoma owing to the high rate of expression o

101 ve detection of urinary HAase activity in 40 bladder carcinoma patients, 11 benign bladder lesions pa

102 dependent data sets of breast, prostate, and bladder carcinoma, prediction of pathway activity by the

103 isoforms in both urothelial development and bladder carcinoma progression, with DeltaNp63 acting as

104 y extracts using tissue from four high-grade bladder carcinomas resulted in no accurate join formatio

105 Finally, analysis of 202 human bladder carcinomas revealed a new categorization of inva

106 This SERS nanoprobe platform makes primary bladder carcinoma screening from in vitro to ex vivo mor

107 Bladder carcinomas selectively down-regulate miRNAs that

108 sion of COX isoforms in benign tissue and in bladder carcinoma specimens.

109 the 253J B-V cell line, a tumorigenic human bladder carcinoma subline.

110 ee discrete regions of 3p were identified in bladder carcinoma, suggesting the involvement of candida

111 of COX-2 in a high percentage of high-grade bladder carcinomas, suggesting a possible role of COX-2

112 ine cervical carcinomas and nine of 26 (35%) bladder carcinomas, suggesting that constitutive activat

113 In human bladder carcinoma (T-24) cells, inhibition of PKC-alpha

114 umor-suppressor gene alterations in invasive bladder carcinoma than in superficial disease, suggestin

115 ence of urothelial carcinoma and the risk of bladder carcinoma, the long-term patient and kidney graf

116 e diagnosis, monitoring, and surveillance of bladder carcinoma, this study aimed to develop and test

117 ession in a series of patients with stage T1 bladder carcinoma treated with a contemporary therapeuti

118 A 67-year-old man with a history of bladder carcinoma was admitted to the emergency departme

119 of 83 consecutive patients in whom stage T1 bladder carcinoma was diagnosed at the Mayo Clinic betwe

120 Among all cancer subtypes, only bladder carcinoma was significantly associated with PV r

121 In bladder carcinoma, we recently identified FGFR3 mutation

122 uced by benign and malignant compartments of bladder carcinomas where it functions to suppress bladde

123 with recurrent superficial transitional cell bladder carcinoma who experienced prior intravesical the

124 h mouse model resembling clinically advanced bladder carcinoma with UMUC3 and NIH 3T3 cells have high

125 ma in situ of the SV40T mice into high-grade bladder carcinomas, without triggering tumor invasion.